Pulmonary Aspiration

Beck‐Schimmer, Beatrice; Rosenberger, Dorothea; Neff, Simona B; Jamnicki, Marina; Suter, Dominik; Führer, Thomas; Schwendener, Reto A.; Booy, Christa; Reyes, Livia; Pasch, Thomas; Schimmer, Ralph C.

doi:10.1097/00000542-200509000-00019

Cited by 29 publications

(14 citation statements)

References 39 publications

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“…Particularly the finding of group necrosis, and massive intracellular, as well as extracellular, edema in the tissue samples shows the intensity of the cell damage. Our findings of histocytes and macrophages in all organs confirms a study by Beck-Schimmer, who described that rat alveolar macrophages play an essential role in the inflammatory response after acid-induced lung injury [30]. Similar results have been described in small animals [8,23].…”

Section: Discussionsupporting

confidence: 92%

Effects of pulmonary acid aspiration on the lungs and extra-pulmonary organs: a randomized study in pigs

et al. 2012

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IntroductionThere is mounting evidence that injury to one organ causes indirect damage to other organ systems with increased morbidity and mortality. The aim of this study was to determine the effects of acid aspiration pneumonitis (AAP) on extrapulmonary organs and to test the hypothesis that these could be due to circulatory depression or hypoxemia.MethodsMechanically ventilated anesthetized pigs were randomized to receive intrabronchial instillation of hydrochloric acid (n = 7) or no treatment (n = 7). Hydrochloric acid (0.1 N, pH 1.1, 2.5 ml/kg BW) was instilled into the lungs during the inspiratory phase of ventilation. Hemodynamics, respiratory function and computer tomography (CT) scans of lung and brain were followed over a four-hour period. Tissue samples of lung, heart, liver, kidney and hippocampus were collected at the end of the experiment.ResultsAcid instillation caused pulmonary edema, measured as increased extravascular lung water index (ELWI), impaired gas exchange and increased mean pulmonary artery pressure. Gas exchange tended to improve during the course of the study, despite increasing ELWI. In AAP animals compared to controls we found: a) cardiac leukocyte infiltration and necrosis in the conduction system and myocardium; b) lymphocyte infiltration in the liver, spreading from the periportal zone with prominent areas of necrosis; c) renal inflammation with lymphocyte infiltration, edema and necrosis in the proximal and distal tubules; and d) a tendency towards more severe hippocampal damage (P > 0.05).ConclusionsAcid aspiration pneumonitis induces extrapulmonary organ injury. Circulatory depression and hypoxemia are unlikely causative factors. ELWI is a sensitive bedside parameter of early lung damage.

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Section: Discussionsupporting

confidence: 92%

Effects of pulmonary acid aspiration on the lungs and extra-pulmonary organs: a randomized study in pigs

et al. 2012

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“…27,29,32,33 The increase in myeloperoxidase activity in the contralateral lung could be attributed to circulating mediators release from the site of injury. 29,32 In addition, in the injured lung, myeloperoxidase activity at 6 h did not differ between the HCl and NaCl groups, as reported in other studies, 21,29 whereas its kinetic in the following period did. In fact, neutrophilic infiltration progressively decreased in the NaCl group, whereas it remained relatively constant in the HCl group.…”

Section: Discussionsupporting

confidence: 53%

Lung Injury and Recovery in a Murine Model of Unilateral Acid Aspiration

Amigoni

Bellani²,

Scanziani

et al. 2008

Anesthesiology

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“…In addition, gastric particles have been found to contribute to lung injury [6]. Previous in vivo and in vitro studies have shown that acid aspiration causes an IL-6 and IL-8 mediated neutrophil influx into the lungs [2, 3, 7, 8]. A correlation between acid aspiration, increased IL-8 levels, and airway neutrophil counts has been found in asthma patients [9].…”

Section: Introductionmentioning

confidence: 99%

Cytotoxicity and Induction of Inflammation by Pepsin in Acid in Bronchial Epithelial Cells

Bathoorn

Daly

Gaiser

et al. 2011

International Journal of Inflammation

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Introduction. Gastroesophageal reflux has been associated with chronic inflammatory diseases and may be a cause of airway remodelling. Aspiration of gastric fluids may cause damage to airway epithelial cells, not only because acidity is toxic to bronchial epithelial cells, but also since it contains digestive enzymes, such as pepsin. Aim. To study whether pepsin enhances cytotoxicity and inflammation in airway epithelial cells, and whether this is pH-dependent. Methods. Human bronchial epithelial cells were exposed to increasing pepsin concentrations in varying acidic milieus, and cell proliferation and cytokine release were assessed. Results. Cell survival was decreased by pepsin exposure depending on its concentration (F = 17.4) and pH level of the medium (F = 6.5) (both P < 0.01). Pepsin-induced interleukin-8 release was greater at lower pH (F = 5.1; P < 0.01). Interleukin-6 induction by pepsin was greater at pH 1.5 compared to pH 2.5 (mean difference 434%; P = 0.03). Conclusion. Pepsin is cytotoxic to bronchial epithelial cells and induces inflammation in addition to acid alone, dependent on the level of acidity. Future studies should assess whether chronic aspiration causes airway remodelling in chronic inflammatory lung diseases.

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Pulmonary Aspiration

Abstract: These data suggest that alveolar macrophages play an essential role in the inflammatory response of acid-induced lung injury. For the first time, attenuation of acid-induced lung injury with an inhibitor, applied after the onset of injury, is shown.

Cited by 29 publications

References 39 publications

Effects of pulmonary acid aspiration on the lungs and extra-pulmonary organs: a randomized study in pigs

Effects of pulmonary acid aspiration on the lungs and extra-pulmonary organs: a randomized study in pigs

Lung Injury and Recovery in a Murine Model of Unilateral Acid Aspiration

Cytotoxicity and Induction of Inflammation by Pepsin in Acid in Bronchial Epithelial Cells

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